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Problem-based Feline Medicine
ed. Jacqui Rand, pub. 2006

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Part 4: Cat with urinary tract signs, page 195
Chapter 12: The Incontinent Cat, by L.J. Filippich

Introduction

Mechanism?

The incontinent cat intermittently or continuously dribbles urine because it has lost voluntary control over urination.

Cats that urinate at inappropriate times or in inappropriate places need to be differentiated from incontinent cats through history taking and clinic examination.

Maintenance of urinary continence in the cat depends on normal lower urinary tract anatomy and an intact sympathetic, parasympathetic and somatic nervous system.

  • Anatomical abnormalities can bypass (ectopic ureter) or negate (urethral hypoplasia) neuromuscular control mechanisms.

Continence during the filling stage is maintained via the following mechanisms: sympathetic stimulation (hypogastric nerve) during the filling phase causes the body of the bladder (detrusor muscle) to relax (β-receptors) and the bladder neck and urethral smooth muscles to contract (α-receptors).

  • Additional urethral resistance is supplied by the urethral striated muscle, which reflexively contracts and is under voluntary control (pudendal nerve).

The emptying phase occurs as follows: Parasympathetic stretch receptors in the detrusor muscle detect bladder fill, and when the threshold of bladder capacity is reached, they discharge impulses via the sacral spinal cord to the pons in the brain stem, where a detrusor response is integrated.

Efferent motor impulses descend the spinal cord to the detrusor muscle via the pelvic nerve causing detrusor muscle contraction.

  • Simultaneously, inhibitory interneurons are activated in the sacral spinal cord, which synapse on pudendal motor neurons, resulting in a relaxation of the external urethral sphincter.

Once the bladder is empty, parasympathetic activity ceases and the sympathetic and pudendal nerves are no longer inhibited.

Detrusor muscle relaxation and urethral sphincter contraction returns and the filling phase begins again.

Incontinence, pollakiuria or nocturia associated with an empty bladder reflect storage disorders (reduced bladder capacity, hyperactivity of the detrusor muscle, urethral incompetence).

In contrast, urine retention with overflow, or incomplete voiding and a distended bladder indicate emptying disorders (detrusor atony, urethral obstruction).

Following spontaneous bladder emptying there should be less than 0.5 ml of urine remaining in a normal cat.

Where?

Lower urinary tract (lower ureter, urinary bladder, urethra).

What?

Urinary incontinence in cats is uncommon. In juvenile cats, it is more likely due to a congenital abnormality (ectopic ureter); in the adult cat it is more likely neurologic in origin. Secondary urinary tract infections are common.

Diseases Causing Signs of Urinary Incontinence

Hypocontractile Bladder***
(Detrusor Atonic / Hypotonic Bladder)

Pathogenesis

Hypocontractile bladder can occur due to detrusor dysfunction or secondary to prolonged bladder distention.

Detrusor dysfunction

  • Lesions cranial to the sacral spinal cord may disrupt sensory and motor pathways to the urinary bladder. This results in an upper motor neuron bladder:
    • Detrusor function is lost resulting in a flaccid bladder.
    • Urethral sphincter tone is maintained.
    • Loss of inhibition may lead to increased pudendal nerve activity and thus, increased urethral outflow resistance.
    • Over time, intrinsic spinal reflexes may re-establish detrusor activity but voiding is usually involuntary and incomplete.
  • Lesions involving the sacral spinal cord segments, cauda equina (sacrum) or peripheral nerves supplying the bladder and urethra result in a lower motor neuron bladder:
    • Loss of most sensory and all motor input to the detrusor muscle.
    • Loss of urethral sphincter tone.
    • The urinary bladder is areflexic and easily expressed.
    • Overflow incontinence occurs when the bladder is distended or when intravesicular pressures exceed urethral pressure.

Prolonged bladder distention

  • Prolonged bladder distention leads to loss of tight muscular junctions in the bladder wall resulting in detrusor atony. Prolonged bladder distention results from reduced bladder emptying which may be from a number of causes:
    • Mechanical (urethroliths, urethral plugs, strictures, bladder neck or urethral masses, inflammation).
    • Functional (neurologic injury, urethral muscle spasm). When bladder fill pressures exceed urethral resistance, overflow of urine occurs.
    • Associated with hindquarter disorders (pain) or forced recumbency.

    Neurologic injury, resulting in urethral hyperactivity/dyssynergia, has been rarely documented in cats. It can occur with sacral spinal cord and cauda equina injuries, resulting in the urethral musculature failing to relax during detrusor contraction, thus maintaining a high outflow resistance.

    Urethral muscle spasm may occur following urethral or pelvic surgery or secondary to urethral inflammatory disease.

    Functional urethral obstruction and detrusor atony are common sequels to mechanical urethral obstruction.

Feline dysautonomia may result in urinary incontinence. There is an inability to contract the bladder and the bladder is easy to express manually. Urinary incontinence is one of the less common signs. Typically there is a sudden onset of depression and anorexia over 24 - 48 hrs, and a variety of signs reflecting autonomic dysfunction, such as pupillary dilation with loss of PLR, dry eyes and nose, regurgitation, prolapsed 3rd eyelids, bradycardia and constipation or fecal incontinence.

Clinical signs

A hypocontractile bladder presents as urinary incontinence associated with a distended urinary bladder and inability to completely void urine.

The cat may or may not voluntarily attempt to urinate.

The bladder may or may not be easily expressed manually.

With suprasacral (cranial to sacrum) spinal cord lesions, the bladder is initially distended, firm and difficult to express.

  • Over time there is emergence of the sacral reflex, and some bladder contractile function may return, resulting in frequent, uninhibited, incomplete voiding of small volumes of urine.
  • If outflow resistance is high at this time, detrusor-urethral dyssynergia occurs resulting in dysuria (difficult or painful urination) and interrupted urination.
  • Other clinical signs associated with suprasacral spinal cord lesions may include proprioceptive deficits, paraparesis or tetraparesis and hyperreflexia.

With sacral spinal cord and peripheral nerve lesions, the urinary bladder is usually distended but flaccid, and outflow resistance is generally low, so the urinary bladder is easily expressed.

  • The cat may attempt to urinate, but fail to produce an adequate stream of urine.
  • Clinical signs may also include hind limb paresis or paralysis, reduced anal tone and perineal reflexes, fecal incontinence and tail paralysis.

Incontinence associated with increased urethral outflow resistance is initially characterised by bladder distention and difficulty in manually expressing urine, a large residual urine volume following voiding, dysuria and an attenuated urine stream (paradoxic incontinence).

If the cat initiates voiding but the urine stream is rapidly interrupted, consider detrusor-urethral dyssynergia.

Fecal incontinence and/or constipation may also be present.

Diagnosis

History may help to characterise the problem, differentiate it from inappropriate urination and identify the possible cause (trauma, prolonged recumbency).

Physical examination

  • Abdominal palpation reveals a distended bladder.
  • If detrusor dysfunction is neurological in origin, other signs of neurological disease such as hindquarter paralysis are commonly seen.

Neurologic examination

  • Neurologic deficits in the limbs suggest a neurologic cause for the incontinence.
  • Loss of anal tone, perineal sensation and tail function indicate a sacral spinal cord lesion.
  • Opthalmological signs (mydriasis) may suggest the incontinence is associated with dysautonomia.

Observe micturition.

  • This should always be done.
  • Note change in bladder size and residual urine volume after voiding.

Detrusor dysfunction is suspected on the basis of the history, physical examination, and the exclusion of a mechanical obstruction to urine outflow.

Catheterise the urinary bladder to determine patency.

  • If an obstruction is detected, survey and contrast radiographs are often necessary to further characterise the obstruction. If the obstruction is due to a urethrolith, survey abdominal radiographs are necessary to determine if other uroliths are present in the urinary tract (kidney, ureter and bladder).
  • If an obstruction is not detected, retrograde urethrography and contrast cystography may be needed to exclude soft tissue masses in the bladder and urethra

If mechanical obstruction is ruled out, subjectively evaluate urethral resistance by palpating the urinary bladder and applying constant, firm digital pressure on the urinary bladder. The degree of pressure applied should not cause undue discomfort or pain to the cat.

  • If detrusor activity is initiated and the cat begins to urinate, observe if the urine stream is abruptly interrupted and voiding is incomplete (functional urethral obstruction).
  • If detrusor activity is not initiated and the bladder is easily expressed, bladder atony is present.

Ultrasonography is often useful in bladder diseases (neoplasia, urolithiasis) but does not visualise most of the urethra.

Urodynamic procedures

  • These are not readily available in veterinary practice.
  • Cystometry, urethral pressure profilometry, uroflowmetry and electromyography can provide useful objective information about detrusor and urethral function.
  • Cystometrography showing large filling volumes, and lack of sustained contractile peaks indicate detrusor atony.
  • Urethral pressure profilometry can identify urethral incompetence and urethral hypertonicity.

Urinalysis is useful in detecting the presence of inflammation and infection.

Blood tests including serum urea, creatinine and electrolyte concentrations can be done to detect renal failure.

Biopsy a soft tissue mass, if detected.

Treatment

Immediately correct any life-threatening conditions, such as post renal failure, and fluid and electrolyte imbalance.

Correct the primary cause, if possible.

Always treat urinary treat infections first before attempting pharmacologic manipulation.

For bladder atony

  • To facilitate smooth muscle recovery, the residual urine volume needs to be kept small by frequent manual expression, intermittent catheterization or temporary indwelling urinary catheter placement.
  • Use pharmacologic manipulation, such as parasympathomimetics (bethanechol chloride, a cholinergic agonist, 1.25 - 2.25 mg/cat orally every 8 - 12 hours) to increase detrusor contractility and an alpha-adrenergic antagonist (phenoxybenzamine, 0.25 mg/kg orally every 12 hours) to minimise urethral resistance, if necessary. Parasympathomimetic drugs are most likely to be effective when some neurologic innervation is still present. Drug doses may be increased incrementally, if needed, every 4–5 days, but patients should be carefully monitored for potential side effects (lacrimation, salivation, abdominal cramps, vomiting, diarrhoea).

For increased urethral resistance or detrusor–urethral dyssynergia.

  • The direct-acting skeletal muscle relaxant, dantrolene sodium (0.5–2 mg/kg orally 12 hourly or 1 mg/kg IV) may be effective in reducing striated-muscle resistance.
  • The alpha-adrenergic antagonist (phenoxybenzamine) may be effective in reducing smooth-muscle resistance.
  • Benzodiazepines such as diazepam (valium 2–5 mg PO tid) may reduce striated-muscle resistance.

Laboratory investigation, including plasma urea, creatinine and electrolyte concentrations and urinalysis, should be done to determine the degree of post-renal azotemia and to identify if hematuria, pyuria and/or infection are present.

Prognosis

Prognosis in neurologic cases is guarded and generally depends on the chronicity and severity of the neurologic lesion, response to medical therapy and the ease of manually maintaining an empty urinary bladder.


Urethral Incompetence*

Pathogenesis

Incontinence occurs because of reduced urethral outflow resistance during urine storage. This results from lost or reduced urethral smooth or striated muscle tone.

Reported causes of urethral incompetence include:

  • Pelvic and pudendal nerve damage following trauma (cystotomy, perineal urethrostomy) and rarely neoplasia (acquired urethral incompetence).
  • Dysraphism in Manx cats.
  • Urethral hypoplasia has been reported in young female cats (congenital urethral incompetence).
  • A relationship between incontinence and feline leukemia virus (FeLV) infection is suspected.
  • Reproductive hormone-responsive incontinence has been reported in two female cats following ovariectomy and suspected in three neutered males.

Clinical Signs

Normal or small urinary bladder.

Intermittent leakage of small volumes of urine, often while the cat is sleeping or relaxed.

If congenital in origin, other anomalies, such as vaginal aplasia and cystic hypoplasia are commonly present.

Many FeLV-positive cats with urinary incontinence may also have anisocoria, reproductive disorders, weight loss, vomiting and ptyalism suggesting a multi-focal autonomic dysfunction. In cats with FeLV-associated incontinence, digital palpation of the urinary bladder often elicits a urine flow.

In cats with urethral incompetence due to neoplasia, abdominal palpation may reveal a mass at the bladder neck. Others signs, such as dysuria and hematuria are often present.

Secondary urinary tract infections are common.

Diagnosis

Diagnosis is based on history and clinical signs of leakage of small amounts of urine, often when sleeping, and a normal or small bladder.

Opthalmological signs (anisocoria) may suggest the incontinence is associated with FeLV infection.

A positive FeLV test.

Retrograde contrast vaginourethrography in female cats with urethral hypoplasia shows marked urethral shortening and other anomalies, such as vaginal aplasia and cystic hypoplasia.

Cystography or retrograde urethrography may reveal a mass at the bladder neck. Biopsy is necessary for a definitive diagnosis.

Urodynamic procedures, including urethral pressure profilometry can be used to identify urethral incompetence.

Differential Diagnosis

Hypercontractile bladder (urge incontinence) is characterised by frequent conscious urination and a small bladder.

Treatment

Bladder neck reconstructive surgery may be considered in cats with urethral hypoplasia.

Alpha-adrenergic agonists, such as phenylpropanolamine (1.5–2.2 mg/kg PO 8–12 h) and ephedrine (2–4 mg/cat PO 8–12 h) may be used to alleviate the incontinence. Once the incontinence is controlled, the dosage can be reduced and/or the frequency lengthened.

High doses of oral oestrogen therapy were reportedly effective in two cats that developed urinary incontinence following ovariectomy. However, at such doses nymphomania and toxic bone marrow effects may occur.

Testosterone propionate (5–10 mg intramuscularly), given to three neutered male cats suspected of reproductive hormone-responsive incontinence, gave variable success.

Prognosis

Response to drug therapy in severely affected animals is often poor.